Mastermind-like 1 | OKDB#: 4091 |
Symbols: | MAML1 | Species: | human | ||
Synonyms: | Mam1, Mam-1, KIAA0200,MASTERMIND, DROSOPHILA, HOMOLOG OF, 1, MAM1 | Locus: | 5q35 in Homo sapiens |
For retrieval of Nucleotide and Amino Acid sequences please go to:
OMIM
Entrez Gene
Mammalian Reproductive Genetics Endometrium Database Resource Orthologous Genes UCSC Genome Browser GEO Profiles new! Amazonia (transcriptome data) new! R-L INTERACTIONS MGI |
General Comment | NCBI Summary: This protein is the human homolog of mastermind, a Drosophila protein that plays a role in the Notch signaling pathway involved in cell-fate determination. There is in vitro evidence that the human homolog forms a complex with the intracellular portion of human Notch receptors and can increase expression of a Notch-induced gene. This evidence supports its proposed function as a transcriptional co-activator in the Notch signaling pathway. [provided by RefSeq] | ||||
General function | Intracellular signaling cascade | ||||
Comment | |||||
Cellular localization | Cytoplasmic | ||||
Comment | |||||
Ovarian function | |||||
Comment | Hedgehog-stimulated stem cells depend on non-canonical activity of the Notch co-activator Mastermind. Vied C et al. Normal self-renewal of follicle stem cells (FSCs) in the Drosophila ovary requires Hedgehog (Hh) signaling. Excess Hh signaling, induced by loss of patched (ptc), causes cell-autonomous duplication of FSCs. We have used a genetic screen to identify Mastermind (Mam), the Notch pathway transcriptional co-activator, as a rare dose-dependent modifier of aberrant FSC expansion induced by excess Hh. Complete loss of Mam activity severely compromises the persistence of both normal and ptc mutant FSCs, but does not affect the maintenance of ovarian germline stem cells. Thus, Mam, like Hh, is a crucial stem cell factor that acts selectively on FSCs in the ovary. Surprisingly, other Notch pathway components, including Notch itself, are not similarly required for FSC maintenance. Furthermore, excess Notch pathway activity alone accelerates FSC loss and cannot ameliorate the more severe defects of mam mutant FSCs. This suggests an unconventional role for Mam in FSCs that is independent of Notch signaling. Loss of Mam reduces the expression of a Hh pathway reporter in FSCs but not in wing discs, suggesting that Mam might enhance Hh signaling specifically in stem cells of the Drosophila ovary. | ||||
Expression regulated by | |||||
Comment | |||||
Ovarian localization | |||||
Comment | |||||
Follicle stages | |||||
Comment | |||||
Phenotypes | |||||
Mutations | 0 mutations | ||||
Genomic Region | show genomic region | ||||
Phenotypes and GWAS | show phenotypes and GWAS | ||||
Links |
|
created: | June 3, 2009, 7:47 a.m. | by: |
hsueh email:
home page: |
last update: | June 3, 2009, 7:48 a.m. | by: | hsueh email: |
Click here to return to gene search form